The mechanisms involved in the normal and abnormal metabolism of sodium have not been entirely defined. Recent studies however suggest that various factors, in addition to glomerular filtration rate and aldosterone activity, may be involved in both the normal excretion and abnormal retention of sodium. Alterations in intrarenal hemodynamics have been demonstrated to constitute one pathway mediating changes in renal sodium reabsorption and these changes in intrarenal hemodynamics may be intergrated into a system regulating extracellular fluid balance predominantly by altering systemic hemodynamics. In the present investigation, various high and low cardiac output models of sodium retention in the dog will be systematically examined with particular attention to integrating alterations in cardiac output total peripheral resistance, arterial pressure, renal vascular resistance and filtration fraction with changes in sodium excretion. Renal denervation, pharmacological depletion of catecholamines, unilateral renal adrenergic blockade, control of renal perfusion pressure and adrenalectomy will be some of the maneuvers utilized to more clearly define the factors involved in these states of sodium retention. In addition, the effect of hematocrit and viscosity on the systemic and renal hemodynamic responses to volume expansion, as well as the renal concentration and diluting mechanism, will be investigated. Lastly, studies will be undertaken to differentiate aerobic, anerobic and passive mechanisms of sodium reabsorption.